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Published on: May 12, 2018
Hyperthermia and the neurotoxicity of exogenous glutamate in infant rats
R Peñafiel1, A Cremades, L Puelles
1Department of Biochemistry, Faculty of Medicine, University of Murcia, Spain.
Insights
High brain glutamate levels, induced by monosodium glutamate or hyperthermia in young rats, reveal that glutamate neurotoxicity requires sustained high extracellular concentrations, not just elevated levels.
Area of Science:
- Neuroscience
- Neurochemistry
- Toxicology
Background:
- Excitatory neurotransmitters like glutamate play crucial roles in brain function.
- Understanding the conditions leading to excitotoxicity is vital for neurological research.
Purpose of the Study:
- To investigate the relationship between elevated brain glutamate levels and neurotoxicity.
- To compare the effects of monosodium glutamate administration versus hyperthermia on brain glutamate and GABA levels and subsequent neurotoxicity.
Main Methods:
- Induction of elevated brain glutamate in 3-day-old rats via monosodium glutamate injection or hyperthermic treatment.
- Measurement of glutamate and GABA levels in rat brains.
- Histological examination for cerebral lesions.
Main Results:
- Both monosodium glutamate and hyperthermia significantly elevated brain glutamate levels.
- Monosodium glutamate treatment also increased GABA levels, unlike hyperthermia.
- Cerebral lesions were observed in glutamate-treated rats but not in hyperthermic rats, despite similar glutamate increases.
Conclusions:
- High extracellular glutamate concentrations are necessary to induce neurotoxic effects.
- The presence of elevated GABA levels may modulate or prevent glutamate-induced neurotoxicity.
- Hyperthermia-induced glutamate elevation, without significant GABA increase, does not lead to observable neurotoxicity, suggesting a threshold effect.
Abstract:
A substantial elevation of the excitatory neurotransmitter glutamate can be produced in the brain of 3-day old rats, either after subcutaneous injection of monosodium glutamate (4 mg/g), or by hyperthermic treatment (40 degrees C, 3 h). In the glutamate-treated animals a large increase in the GABA levels has also been observed while the elevation of this amino acid in the hyperthermic animals is insignificant. Although the magnitude of the increase of glutamate in both cases is rather similar, in the hyperthermic animals no cerebral lesions such as those produced in the glutamate-treated animals could be observed. Therefore, high extracellular levels of glutamate seem to be required to produce the variety of neurotoxic effects related to this excitatory amino acid.
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